The Effect of Azelastine on Exercise-Induced Asthma

Magnussen, H; Reuss, Gabriele; Jörres, Rudolf A.; Aurich, R

doi:10.1378/chest.93.5.937

Cited by 29 publications

(6 citation statements)

References 13 publications

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“…In-vitro studies of human lung mast cells show that increasing the osmolarity of the solution bathing the cells is a potent stimulus to release of histamine [17]. The major clinical evidence to support a role for histamine release is the finding that some histamine H1 receptor antagonists have an inhibitory effect on exercise-induced bronchoconstriction (EIB) [18][19][20]. Because the inhibitory effect is incomplete, histamine cannot be the only mediator involved in EIB.…”

Section: Mechanisms and Receptors Involved In Indirect Challengesmentioning

confidence: 99%

Indirect airway challenges

Joos

O’Connor²,

Anderson³

et al. 2003

Eur Respir J

327

274

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Indirect challenges act by causing the release of endogenous mediators that cause the airway smooth muscle to contract. This is in contrast to the direct challenges where agonists such as methacholine or histamine cause airflow limitation predominantly via a direct effect on airway smooth muscle.Direct airway challenges have been used widely and are well standardised. They are highly sensitive, but not specific to asthma and can be used to exclude current asthma in a clinic population. Indirect bronchial stimuli, in particular exercise, hyperventilation, hypertonic aerosols, as well as adenosine, may reflect more directly the ongoing airway inflammation and are therefore more specific to identify active asthma. They are increasingly used to evaluate the prevalence of bronchial hyperresponsiveness and to assess specific problems in patients with known asthma, e.g. exercise-induced bronchoconstriction, evaluation before scuba diving.Direct bronchial responsiveness is only slowly and to a modest extent, influenced by repeated administration of inhaled steroids. Indirect challenges may reflect more closely acute changes in airway inflammation and a change in responsiveness to an indirect stimulus may be a clinically relevant marker to assess the clinical course of asthma. Moreover, some of the indirect challenges, e.g. hypertonic saline and mannitol, can be combined with the assessment of inflammatory cells by induction of sputum.

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Section: Mechanisms and Receptors Involved In Indirect Challengesmentioning

confidence: 99%

Indirect airway challenges

Joos

O’Connor²,

Anderson³

et al. 2003

Eur Respir J

327

274

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“…For example, disodium cromoglycate (DSCG), a drug which stabilizes mast cell membranes, is effective in blunting exercise-induced asthma [6,7]. Pretreatment with a number of H 1 receptor antagonists has been shown to attenuate EIB [8][9][10]; however, the degree of protection afforded by this class of drugs has been modest. More recently, studies employing leukotriene receptor antagonists [11,12] and biosynthesis inhibitors [13] have implicated leukotrienes in the airway bronchoconstrictor response to exercise.…”

mentioning

confidence: 99%

Evidence for mast cell activation during exercise-induced bronchoconstriction

O’Sullivan¹,

Roquet²,

Dahlén³

et al. 1998

Eur Respir J

125

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Exercise-induced bronchoconstriction (EIB) is thought to occur in 70-80% of asthmatics, most commonly amongst those with moderate-to-severe airway hyperresponsiveness [1]. It is characterized by transient airflow obstruction resulting in a Š15% decrease in forced expiratory volume in one second (FEV1) following 5-8 min of exercise. The fall in FEV1 reaches a maximum approximately 10 min after exercise and gradually normalizes over the next hour [2]. The precise pathophysiology of EIB remains unclear, although it is widely accepted that during exercise the upper airways are unable to adequately warm and humidify the increased volumes of inspired air. This results in airway cooling and increased airway fluid osmolality in the lower airways [3,4]. One hypothesis suggests that hyperosmolar triggering of mast cells and possibly other inflammatory cells results in the release of bronchoconstricting mediators, e.g. cysteinyl-leukotrienes (cys-LTs), histamine and prostaglandin (PG)D 2 [5].Previous indications for the participation of mast cell mediators in the pathogenesis of EIB are based on pharmacological data. For example, disodium cromoglycate (DSCG), a drug which stabilizes mast cell membranes, is effective in blunting exercise-induced asthma [6,7]. Pretreatment with a number of H 1 receptor antagonists has been shown to attenuate EIB [8][9][10]; however, the degree of protection afforded by this class of drugs has been modest. More recently, studies employing leukotriene receptor antagonists [11,12] and biosynthesis inhibitors [13] have implicated leukotrienes in the airway bronchoconstrictor response to exercise.The direct approach of measuring mast cell mediator release in response to exercise challenge has yielded ambiguous results. Some studies have reported an elevation in plasma and whole blood histamine concentrations following EIB [14,15], while other studies have failed to verify those findings [16,17]. Apart from the methodological problems encountered when sampling plasma histamine [18] and its short half-life in the circulation, approximately 1 min [19], it has been suggested that elevations in plasma histamine mainly reflect the basophilia which normally accompanies exercise [20]. Increases in the levels of tryptase and PGD 2 , both specific mast cell markers, have been detected in nasal lavage following nasal provocation with cold dry air [21], but not after exercise [22,23].The purpose of this study was to provide evidence to establish mast cell activation as a feature of EIB. To this end, a combination of mast cell markers, 9α,11β-PGF 2 Sullivan, A. Roquet, B. Dahlén, F. Larsen, A. Eklund, M. Kumlin, P.M. O'Byrne, S-E. Dahlén. ©ERS Journals 1998. ABSTRACT: Controversy remains about the causative mediators in the bronchoconstrictive response to exercise in asthma. This study examined whether mast cell activation is a feature of exercise-induced bronchoconstriction by measuring urinary metabolites of mast cell mediators. Evidence for mast cell activation during exercise-induced bronchoconstriction....

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“…However, results of studies with the more potent, newer H 1 receptor antagonists in EIA have been varied. Inhaled cetirizine, 3 oral azelastine, 4 and higher doses of terfenadine, 5 have been reported to protect against EIA, whereas ketotifen failed to show any effect. 6 In the present study, the fall in FEV 1 after exercise was statistically reduced by loratadine.…”

Section: Discussionmentioning

confidence: 99%

The effect of loratadine in exercise-induced asthma

Baki

Orhan²

2002

Archives of Disease in Childhood

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Aims: To assess the effect of loratadine in exercise induced asthma. Methods: Randomised, double blind, placebo controlled study of 10 mg oral loratadine, once daily for three days in 11 children. At the end of the treatment period FEV 1 was measured, and patients were exercised on a treadmill. FEV 1 measurements were repeated at intervals after exercise. Results: Loratadine significantly reduced the decrease in FEV 1 after exercise at two, five, 10, 15, and 30 minutes, compared with placebo (p < 0.05). However, the mean decrease in FEV 1 at five minutes was more than 15% of baseline in the loratadine group. Conclusions: Loratadine reduces, but does not prevent, exercise induced asthma in children. E xercise induced asthma (EIA) is defined as a reduction of 15% or more in forced expiratory volume in one second (FEV 1 ) after exercise, and is known to occur in 70-80% of asthmatic children. 1Loratadine is a long acting, highly selective histamine H 1 receptor antagonist, and possesses some anti-inflammatory activity. Loratadine is protective against histamine induced bronchoconstriction, and inhibits allergen induced early and late phase airway obstruction in asthmatics. Recent studies have shown that loratadine produces a mild bronchodilatation, and is effective in the long term treatment of allergic asthma. 2 We investigated the effect of a 10 mg oral dose of loratadine, once daily for three days, on EIA in children, as we are unaware of any studies of its effects on EIA in the paediatric population. METHODSFourteen children (eight boys, six girls; mean age 11.45 (SE 0.87) years, range 7-17) with bronchial asthma, diagnosed within the past month, were studied. All patients were judged atopic on the basis of positive skin tests to common allergens other than pollens, and increased serum concentrations of total and specific IgE. All patients had a history of exercise induced asthma, and had been previously shown to develop airway obstruction after exercise on a treadmill. To avoid the probable influences of seasonal allergies, patients with pollen allergies were excluded. Patients were excluded if they had symptoms or physical signs suggestive of renal, hepatic, or cardiovascular disease.The lung function entry criterion on the exercise test days was an FEV 1 above 75% of predicted. During the study period, the patients had no medical condition that was likely to interfere with the evaluation of the clinical response to medication. None had a history of intolerance to antihistamines. Patients were symptom free as a result of the use of inhaled corticosteroids (budesonide 200 µg twice daily in seven, fluticasone propionate 125 µg twice daily in seven) with a baseline FEV 1 above 85% (SE 3.4%) of predicted normal. The inhaled corticosteroids were discontinued one week before the study period and no medication other than short acting β 2 adrenergic agonists was allowed during the trial. No patients had taken oral steroids or antihistamines in the past three months. None were using cromolyn sodium, long acting β 2 adr...

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The Effect of Azelastine on Exercise-Induced Asthma

Cited by 29 publications

References 13 publications

Indirect airway challenges

Indirect airway challenges

Evidence for mast cell activation during exercise-induced bronchoconstriction

The effect of loratadine in exercise-induced asthma

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